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Pathology Flashcards

1
Q

Three steps of acute inflammation

A

Vascular: dilation of vessels
Exudative: vascular leakage of protein rich fluid
Cells recruited: neutrophil polymorphs

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2
Q

Causes of acute inflammation

A

Microbial infections e.g. bacteria
Hypersensitivity reactions e.g. parasites
Physical agents e.g. heat
Chemicals e.g. acid

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3
Q

Neutrophil polymorph emigration

A

Margination of neutrophils
Adhesion of neutrophils (pavementing)
Neutrophil emigration
Diapedesis (leukocyte extravasation)

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4
Q

Outcomes of acute inflammation

A

Resolution: complete restoration of tissues e.g. acute lobar pneumonia

Suppuration: formation of pus, leads to scarring

Organisation: replacement by granulation tissue, macrophages migrate, fibrosis occurs e.g. post-MI

Progression: causative agent is not removed, progresses to chronic

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5
Q

Cells involved in acute inflammation

A

Neutrophils: phagocytose pathogens
Monocytes: migrate to tissue and become macrophages which induce chemotaxis

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6
Q

Cells involved in chronic inflammation

A

Lymphocytes, macrophages, plasma cells

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7
Q

Macroscopic appearance of chronic inflammation

A

Chronic ulcer
Chronic abscess cavity
Granulomatous inflammation
Fibrosis

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8
Q

Cellular cooperation in chronic inflammation

A

B lymphocytes: plasma cells, antibody production
T lymphocytes: cell-mediated immunity
Macrophages: respond to chemotactic stimuli, cytokine production (interferon alpha and beta, IL1, IL6, IL8, TNF-alpha)

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9
Q

Granulomas

A

An aggregate of epithelioid histocytes (activated macrophages resembling epithelial cells)

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10
Q

Causes of granuloma development

A

TB (most common)
Leprosy
Chrons
Sarcoidosis

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11
Q

Granuloma and eosinophil presence

A

Parasite

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12
Q

Platelet alpha granules

A

Platelet adhesion e.g. production of fibrinogen, vWF

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13
Q

Platelet dense granules

A

Platelet aggregation e.g. ADP

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14
Q

First stage of thrombus formation

A

Platelet aggregation (starts the clotting cascade)

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15
Q

Three major causes of thrombosis (Virchow’s triad)

A

Reduced blood flow (stasis) e.g. immobility

Blood vessel/endothelial injury e.g. trauma, HT

Hypercoagulability e.g. smoking

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16
Q

Arterial thrombosis formation

A

Atheromatous plaque causes turbulence in blood flow
Loss of endothelial cells, exposure to collagen
Platelet adherence and activation
Thrombus: platelets > fibrin > RBCs
Grows in the direction of blood flow (propagation)

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17
Q

Venous thrombosis patho

A

Lower blood pressure in veins, atheroma do not occur
Thrombi begin at valves which produce a degree of turbulence and can be damaged e.g. stasis
Formed under low blood pressure
Mainly made of RBCs

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18
Q

Clinical features of arterial thrombi

A

Loss of pulse distal to thrombus
Area becomes cold, pale and painful
Possible gangrene

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19
Q

Clinical features of venous thrombi

A

Tender

Area becomes reddened and swollen

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20
Q

Complications of arterial thrombus and treatment

A

MI/stroke

Tx: anti-platelets e.g. aspirin

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21
Q

Complications of venous thrombus and treatment

A

DVT/PE

Tx: anti-coagulants e.g. warfarin

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22
Q

Pulmonary embolism

A

Venous emboli travel to vena cava and lodge in the pulmonary arteries

Presentation:
Acute respiratory or cardiac problems
Chest pain and shortness of breath

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23
Q

Ischaemic reperfusion injury

A

Damage to tissue during reoxygenation after a period of ischaemia

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24
Q

Atherosclerosis pathogenesis

A

High levels of LDL accumulates IN arterial wall

Macrophages and T-cells are attracted to the site of damage and take up lipid to form foam cells

Formation of fatty streak

Activated macrophages release cytokines and growth factors

Smooth muscle cell proliferation around the lipid core, thinning of tunica media

Formation of a fibrous cap (collagen)

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25
Risk factors for atherosclerosis
``` Hypercholesterolaemia (prevention: statins) Smoking Hypertension Diabetes Male ```
26
Apoptosis
Programmed sequence of intracellular events leading to the removal of a cell without the release of harmful products to surrounding cells
27
Inhibitors of apoptosis
Growth factors ECM Sex steroids
28
Inducers of apoptosis
Glucocorticoids Free radicals Ionising radiation DNA damage
29
Intrinsic apoptosis pathway
Mitochondrial pathway: Biochemical stress e.g. free radicals Bax: induces apoptosis (p35 cell cycle arrest) Activation of caspase cascade
30
Extrinsic apoptosis pathway
Used by the immune system to eliminate lymphocytes Ligand binding at death receptors on cell surface Receptors include TNFR1 (TNF-alpha ligand) and Fas receptor (Fas ligand) Activation of caspase cascade
31
Necrosis
Traumatic cell death which indices inflammation and repair | Characterised by bioenergetic failure and loss of plasma membrane
32
Coagulative necrosis
Most common type Can occur in most organs but most commonly heart and kidneys Caused by hypoxia (ischaemia)
33
Liquefactive necrosis
Hydrolytic enzymes | Occurs in the brain due to its lack of substantial supporting stroma e.g. stroke
34
Caseous necrosis
Causes a cottage cheese pattern | TB is characterised by this form of necrosis
35
Gangrene
Necrosis with rotting of the tissue | Affected tissue appears black due to deposition of iron sulphide (from degraded haemoglobin)
36
Fat necrosis
Fatty acids spill out of adipose cells | Pancreatitis
37
Fibrinoid necrosis
Fibrin deposits | Vasculitis
38
Hypertrophy
Increase in cell SIZE without cell division | E.g. muscle hypertrophy in athletes, uterine hypertrophy in pregnancy
39
Hyperplasia
Increase in cell number by division (mitosis) | Cannot happen in cells that don’t divide i.e. myocardial cells or nerve cells
40
Atrophy
Decrease in the size of an organ - can be a reduction in cell size or cell number E.g. muscle atrophy in ALS
41
Metaplasia
Change in the DIFFERENTIATION of a cell Occurs in response to alterations in the cellular environment E.g. squamous epithelium > columnar epithelium in Barrett’s oesophagus
42
Dysplasia
Morphological changes seen in cells in the progression to BECOMING CANCER
43
Carcinogenesis
Transformation of normal cells into neoplastic (cancerous) cells through permanent genetic alterations or mutations
44
Why can neoplasms not arise in erythrocytes
No nuclei
45
Tumour
Any abnormal swelling
46
Carcinogen examples
Smoking - lung tumours EBV - Burkitts lymphoma HPV - cervical cancer UV radiation - skin cancer
47
Benign tumours features
``` Do not invade basement membrane Exophytic (grow outwards) Low mitotic activity Circumscribed (limited to an area) Necrosis and ulceration are rare ```
48
Malignant tumours
``` Invade the basement membrane Endophytic (grows inwards) High mitotic activity Poorly circumscribed Necrosis and ulceration are common ```
49
Benign epithelial tumours
Papilloma (non glandular) | Adenoma (glandular secretory tissue)
50
Malignant epithelial tumours
Carcinoma (malignant tumour of epithelial cells) | Adenocarcinoma (malignant tumour of glandular epithelial cells)
51
Types of benign connective tissue tumours
``` Lipoma: adipocytes Rhabdomyoma: skeletal muscle Leiomyoma: smooth muscle cells Chondroma: cartilage Osteoma: bone ```
52
Malignant connective tissue tumours
``` Liposarcoma: adipocytes Rhabdomysaroma: skeletal muscle Leiomysaroma: smooth muscle cells Chondrsaroma: cartilage Ostesarcoma: bone ```
53
Metastasis | which cancer never metastasises?
Malignant tumours spread from their site of origin to form other tumours at distant cites Basal cell carcinoma NEVER metastasises
54
Bone metastasises from
Lung, breast, kidney, thyroid, prostate
55
Carcinomas preferred route
Lymphatic spread
56
Sarcoma preferred route
Haematogenous spread
57
Define inflammation
A local physiological response to injury
58
Most common cause of chronic inflammation
Primary chronic inflammation
59
Epitheliod histiocytes
Activated macrophages that resemble epithelial cells Aggregation = granuloma
60
Sarcoidosis
Occurs when inflammatory cells clump together to form granulomas
61
Blood marker in the investigation if sarcoidosis
Serum ACE
62
Sequence of events in metastasis
Invasion: erosion of tissue boundaries Intravasion: gain access to metastatic routes e.g. lymph Evasion of host defence Adherence to endothelium Extravasation: colonisation of new site Angiogenesis: develops its own blood supply
63
Primary pulmonary neoplasm to liver, via which spread?
Haematogenous spread
64
Bcl-2 role in apoptosis
Inhibits apoptosis
65
CO2 reading on an ABG
Same direction as pH = metabolic | Opposite direction = respiratory

Belle Phase 2a (14 decks)

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